ArticleJournal of controlled release : official journal of the Controlled Release Society2026
Narrowing of glioma vascular caliber via chronic VEGFR2 blockade improves the uniformity of focused ultrasound-mediated small molecule drug delivery.
Article in Journal of controlled release : official journal of the Controlled Release Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Glioblastoma (GBM) is a devastating disease, with standard-of-care therapies still yielding dismal survival outcomes. GBM cells are protected by the blood-brain and blood-tumor barriers, which severely limit therapeutic agent delivery from the bloodstream. Focused ultrasound (FUS), in combination with microbubbles (MBs), addresses this challenge by enhancing drug delivery. However, dilated and tortuous brain tumor vasculature disrupts MB flux and oscillation, which may limit FUS-mediated delivery. Here, we evaluated whether normalizing tumor vasculature via chronic neoadjuvant VEGFR2 inhibition (aVEGFR2, DC101) improves subsequent FUS-mediated small molecule drug delivery. After aVEGFR2 administration had pre-normalized GL261 glioma vasculature through reduced permeability and vascular caliber, T1 mapping MRI of FUS-delivered Multihance (MH) contrast agent, a model small molecule drug, yielded no change in total delivery. However, radiomic analysis of the T1 maps indicated that FUS-mediated model drug penetration into otherwise poorly accessible tumor regions was improved with aVEGFR2 pre-treatment. This improvement was accompanied by acoustic signatures suggestive of more stable MB oscillation. These results were then compared to those achieved with acute aVEGF pre-treatment, a regimen that copied the permeability reduction of chronic aVEGFR2 without reducing vascular caliber. This comparison identified reduced vascular caliber as the probable mechanism of improved delivery uniformity, perhaps acting through a shift in MB oscillation towards more stable regimes. Our results indicate that neoadjuvant aVEGFR2 cooperates with FUS-mediated small molecule drug delivery through a unique biophysical mechanism. This mechanism may be leveraged to further augment the efficacy of combination therapies against GBM that entail blocking VEGF signaling.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.